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sensitivities ranging from 93% to 100%, and specificities
from 76% to 100%(11). However , false-positives include
cases of pyothorax and other diseases such as lung
cancer, lymphoma and pleural mesothelioma. False-negatives
may be either in an early stage of tuberculous
pleurisy or in a state of insufficient immunity (23). The
results of the present study also showed the ADA levels
in the tuberculous group to be significantly higher than in
the malignant and inflammatory groups. As described
Figure 4
IFNγ (IU ml -1 ) in pleural effusions. Mean ( ⎯ ), cut-off (-----), ** p < 0.01
Figure 5
ROC curves for diagnosis of tuberculosis. AUC: area under the curve. IFNγ showed a maximal
area (0.987). ADA, TNFα and IL-8 recorded 0.927, 0.897 and 0.702, respectively
previously , ADA seems to be a useful marker of tuberculous
pleurisy.
It has been reported that , in patients with tuberculous
pleurisy, cell - mediated immunity participates in protection
against infection with tubercle bacilli, and IL-1, -8, -10, -12,
TNF- α and IFN- γ are produced (25,26).
IL-8, which stimulates T cells, is known to play an
important role in granulomatous process (27). Production
of IL-8 by monocytes after phagocytizing tubercle bacilli
has been described (28), but
some researchers reported
high levels in pleural fluid associated
with either pyothorax
or pneumonia, correlating
with neutrophil counts
and extent of myeloperoxidase
activity (29,30). In one
report IL-8 elevation was
found to be greater with pyothorax
or pneumonia than
with tuberculosis or malignancy
(31). In our study IL-
8 was particularly elevated in
the tuberculous group & this
was significantly high when
compared to the malignant
group but not the inflammatory
group. The reasons for
the discrepancies are still
unclear and may depend on
the timing of specimen collection
or other factors but
clearly, IL-8 is not optimal as
a diagnostic marker.
Higher TNF- α levels in
tuberculous as compared to
the other groups were found
in this study as in other studies
(32,33). TNF- α is considered
necessary for producing
granulomas and removing
rod-shaped bacteria
in inflammatory lesions, and
it is also regarded as an inducer
of IFN- γ. In rheumatic
pleural effusion , TNF- α increases
in a similar manner
as in the tuberculous case.
However down-regulation of
IFN- γ production occurs in
rheumatic pleural liquid (34).
A number of researchers
have reported that distinction
of tuberculous from
rheumatic or inflammatory
pleural effusion cannot be
made with TNF- α (34).
The T lymphocyte re-
biochimica clinica, 2005, vol. 29, n. 1 17